Studies are continuing on the phenomenology associated with the action of streptomycin (SM) and several other aminoglycoside antibiotics on E. coli. Studies are underway of several models and suggestions for the site at which SM interrupts the normal cycle of ribosome function. Much effort is also being devoted to obtaining a better understanding of the various phenotypes produced by mutations at the str locus, and by the genetic suppression of these mutations. The question of ribosome turnover and biogenesis is also being explored as there appears to be an assembly defect in a majority of these mutants.